Objective Determine the risk posed by cochlear implantation (CI) to the labyrinth. Study Design Prospective cohort study. Setting Academic tertiary referral center. Patients Thirty-six ears belonging to 35 adult CI candidates (mean: 46, range: 23–69 years old). Intervention Cochlear implantation. Main Outcome Measures Vestibular function was assessed using the quantitative 3D head impulse test (qHIT), clinical head impulse test (cHIT), post-headshake nystagmus (HSN), caloric electronystagmography (ENG), vestibular-evoked myogenic potentials (VEMP), dynamic visual acuity (DVA), and Dizziness Handicap Inventory (DHI). Results All 36 ears were tested using qHIT before CI, and 28 ears were tested 4–8 weeks after CI. Quantitative HIT showed 1/28 of ears suffered reduced function. Clinical HIT was 44% sensitive and 94% specific for identification of severe-to-profound vestibular hypofunction confirmed by qHIT. HSN was unchanged in 11/11 subjects. New hyporeflexia was found in 1/16 of ENG-tested ears. VEMP showed either a disappearance of response or an increase in threshold by >10dB in 5/16 ears. Passive DVA showed no change in 16/16 ears. DHI scores worsened in 3/28 and improved in 4/28 subjects. Conclusions Although small, the observed rate of labyrinthine injury was comparable to that for other risks of CI. Thus, it is important to educate CI candidates about possible risk to balance function, particularly when CI of an “only balancing ear” is contemplated. Clinical HIT is useful for detecting severe high-frequency vestibular hypofunction and should be part of the pre-CI physical examination.

By sensing three-dimensional (3D) head rotation and electrically stimulating the three ampullary branches of a vestibular nerve to encode head angular velocity, a multichannel vestibular prosthesis (MVP) can restore vestibular sensation to individuals disabled by loss of vestibular hair cell function. However, current spread to afferent fibers innervating non-targeted canals and otolith endorgans can distort the vestibular nerve activation pattern, causing misalignment between the perceived and actual axis of head rotation. We hypothesized that over time, central neural mechanisms can adapt to correct this misalignment. To test this, we rendered five chinchillas vestibular-deficient via bilateral gentamicin treatment and unilaterally implanted them with a head mounted MVP. Comparison of 3D angular vestibulo-ocular reflex (aVOR) responses during 2 Hz, 50°/s peak horizontal sinusoidal head rotations in darkness on the first, third and seventh days of continual MVP use revealed that eye responses about the intended axis remained stable (at about 70% of the normal gain) while misalignment improved significantly by the end of one week of prosthetic stimulation. A comparable time course of improvement was also observed for head rotations about the other two semicircular canal axes and at every stimulus frequency examined (0.2–5 Hz). In addition, the extent of disconjugacy between the two eyes progressively improved during the same time window. These results indicate that the central nervous system rapidly adapts to multichannel prosthetic vestibular stimulation to markedly improve 3D aVOR alignment within the first week after activation. Similar adaptive improvements are likely to occur in other species, including humans.

Facial paralysis represents the end result of a wide array of disorders and heterogeneous etiologies, including congenital, traumatic, infectious, neoplastic, and metabolic causes. Thus, facial palsy has a diverse range of presentations, from transient unilateral paresis to devastating permanent bilateral paralysis. Although not life-threatening, facial paralysis remains relatively common and can have truly severe effects on one's quality of life, with important ramifications in terms of psychological impact and physiologic burden. Prognosis and outcomes for patients with facial paralysis are highly dependent on the etiologic nature of the weakness as well as the treatment offered to the patient. Facial plastic surgeons are often asked to manage the sequelae of long-standing facial paralysis. It is important, however, for any practitioner who assists this population to have a sophisticated understanding of the common etiologies and initial management of facial paralysis. This article reviews the more common causes of facial paralysis and discusses relevant early treatment strategies.